Sphingosine 1-phosphate regulates inflammation-related genes in human endothelial cells through S1P1 and S1P3

被引：54

作者：

Lin, Chi-Iou

Chen, Chiung-Nien

Lin, Po-Wei

Lee, Hsinyu

机构：

[1] Natl Taiwan Univ, Inst Zool, Taipei 106, Taiwan

[2] Natl Taiwan Univ, Angiogenesis Res Ctr, Taipei 106, Taiwan

[3] Natl Taiwan Univ Hosp, Dept Surg, Taipei 106, Taiwan

[4] Acad Sinica, Ctr Appl Sci, Div Mech, Taipei 115, Taiwan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2007年 / 355卷 / 04期

关键词：

S1P; S1P(1); S1P(3); endothelial cells;

D O I：

10.1016/j.bbrc.2007.02.043

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Sphingosine 1-phosphate (S1P) is a bioactive lysophospholipid (LPL) ligand that binds endothelial differentiation gene (Edg) family G-protein-coupled receptors and has been implicated as an important regulator in endothelial cells during inflammation processes. In this study, we attempt to determine which SIP receptors mediating the inflammatory response in human endothelial cells. Our results indicated that introduction of siRNA against SIP, significantly suppressed SIP-induced ICAM-I mRNA, total protein, and cell surface expressions in human umbilical vein endothelial cells (HUVECs). Moreover, U937 cells adhesion to SIP-treated HUVECs was profoundly reduced by knock-down of S1P, in HUVECs. By knock-down of S1P(3) or S1P(3) in HUVECs, S1P-enhanced IL-8, MCP-1 mRNA expression, and THP-l cell chemotaxis toward SIP-treated HUVEC-conditioned media was profoundly reduced. These results suggested that SIP-induced inflammatory response genes expression is mediated through S1P(1) and S1P(3). Our findings suggest the possible utilization of S1P, or S1P(3) as drug targets to treat severe inflammation. (c) 2007 Elsevier Inc. All rights reserved.

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页码：895 / 901

页数：7

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